Renal R2 chemoreceptor activity is attenuated after back heating in the rat

The aim of the present study was to determine the afferent connections of the nucleus accumbens in snakes, in particular its catecholaminergic input. For that purpose, in vitro and in vivo applications of retrograde tracers in the nucleus accumbens of Elaphe guttata were combined with tyrosine hydroxylase (TH) immunohistochemistry. Both techniques revealed telencephalic inputs to the nucleus accumbens originating from the diagonal band of Broca, ventral pallidum, amygdaloid complex, and dorsal cortex. Major diencephalic inputs arise from the dorsomedial thalamic nucleus and the hypothalamus. In the brainstem, a few retrogradely labeled cells were observed in the raphe nucleus and the locus coeruleus. Considerably more cells were found in the midbrain tegmentum. Within the confines of the locus coeruleus and, in particular, the midbrain tegmentum, retrogradely labeled cells stained also for TH suggesting that those areas constitute the major catecholaminergic input to the nucleus accumbens of snakes. The experimental approach used in the present study, in particular the in vitro technique, seems to be very suited for studying the development of basal ganglia organization of reptiles in the near future.     

Decreased fecal bile acid output in patients with coronary atherosclerosis

In most patients with atherosclerosis, the underlying metabolic derangement remains undefined. Animal experiments have suggested that the ability to produce and excrete large amounts of bile acids may be an adaptation mechanism to cholesterol overload protecting against the atherogenic effects of cholesterol. However, there are very few data on bile acid excretion in human atherosclerosis. In the present study, we have investigated fecal bile acid secretion in subjects with and without coronary artery disease. The target group consisted of 30 patients with proven coronary artery disease and the control group consisted of 27 matched subjects without clinical or laboratory evidence of coronary atherosclerosis. Fecal bile acids were measured by gas-liquid chromatography from 24-hr stool collections under a controlled diet. The patients excreted significantly less bile acids than the controls (325+/-135 vs. 592+/-223 mg/day, respectively, p < 0.0001). The difference was primarily due to a reduced excretion of secondary bile acids. Less than 50% of deoxycholate was excreted by patients (180+/-81 mg/day) as compared to controls (367+/-168 mg/day, p < 0.0002), while lithocholic acid excretion was 111+/-62 mg/day in patients vs. 190 +/-70 mg/day in controls (p < 0.005). The fecal output of the two primary bile acids, cholic and chenodeoxycholic acid, did not differ significantly between patients and controls. The fecal output of total bile acids correlated with that of both secondary bile acids in patients as well as in controls. These findings suggest that patients with coronary heart disease are unable to excrete adequate amounts of bile acids to rid themselves of excess cholesterol, even if they are able to maintain a plasma cholesterol level comparable to that of healthy controls.     

Effect of postischemic reperfusion on microcirculation and lipid metabolism of skeletal muscle

To study the effect of ischemia reperfusion injury on microvascular reactivity and tissue metabolism in skeletal muscle, a Sprague-Dawley rat cremaster muscle was prepared as a tourniquet ischemia model and subjected to 2 hr ischemia followed by 1 hr reperfusion to simulate the timing of ischemia during microvascular surgery. The dose-response curve of arteriolar reactivity to norepinephrine, lipid peroxidation, and ultrastructure of capillaries was determined in both the control and postischemic reperfusion stages. Judging from the results, we summarize our observations as follows: (1) Postischemic reperfusion significantly increased arteriolar reactivity to norepinephrine, in which the EC50 for vasoconstriction decreased in all three orders of arterioles. These results suggest that reperfusion could have impaired the vasodilation control mechanism, possibly being endothelium dependent. (2) Lipid peroxidation increased sixfold in the reperfusion group, suggesting that oxygen free radicals have produced significant tissue damage under the created conditions. (3) Significant endothelial damage in the capillaries shown by electron microscope observation supports these studies, indicating that ischemia/reperfusion in clinically transplanted skeletal muscles could cause significant damage to the tissue microcirculation both physiologically and metabolically.